scholarly journals Effect of Estradiol in an Azoxymethane/Dextran Sulfate Sodium-Treated Mouse Model of Colorectal Cancer: Implication for Sex Difference in Colorectal Cancer Development

2019 ◽  
Vol 51 (2) ◽  
pp. 632-648 ◽  
Author(s):  
Hee Jin Son ◽  
Sung Hwa Sohn ◽  
Nayoung Kim ◽  
Ha-Na Lee ◽  
Sun Min Lee ◽  
...  
2020 ◽  
Vol 182 ◽  
pp. 114279
Author(s):  
Chin-Hee Song ◽  
Nayoung Kim ◽  
Ryoung Hee Nam ◽  
Soo In Choi ◽  
Joo Hee Son ◽  
...  

2019 ◽  
Vol 164 ◽  
pp. 139-151 ◽  
Author(s):  
Chin-Hee Song ◽  
Nayoung Kim ◽  
Sun Min Lee ◽  
Ryoung Hee Nam ◽  
Soo In Choi ◽  
...  

2016 ◽  
Vol 2016 ◽  
pp. 1-11 ◽  
Author(s):  
Isao Okayasu ◽  
Kiyomi Hana ◽  
Noriko Nemoto ◽  
Tsutomu Yoshida ◽  
Makoto Saegusa ◽  
...  

Vitamin A is essential to mucosal immunity and cell differentiation. The fact that lack of it might involve chronic inflammation and increased risk of cancer has been reported. Little is known about the mechanism of vitamin A deficiency in the development of colitis and its influence on development of colorectal cancer. To determine the influence of vitamin A deficiency on colitis and colorectal cancer development, an experimental study using a colitis mouse model was performed. Dextran sulfate sodium (DSS) colitis was induced in vitamin A-deficient and vitamin A-supplemented mice. Further, colorectal carcinoma was induced by a combination of azoxymethane preinjection and DSS colitis. Results were compared between the two groups mainly by immunohistochemical analysis. Colitis was more severe and recovery from colitis was slower in vitamin A-deficient mice than in vitamin A-supplemented mice. Compared with vitamin A-supplemented mice, vitamin A-deficient mice had decreases in colonic subepithelial myofibroblasts and the ratio of mucosal IgA+/IgG+cells, increases in CD11c+dendritic cells, and a higher rate of development of colorectal carcinoma with colitis following azoxymethane. Vitamin A lipid droplets in subepithelial myofibroblasts were decreased in vitamin A-deficient mice, suggesting alterations in colonic crypt niche function. Thus, vitamin A inhibited colitis and the development of colorectal cancer.


Planta Medica ◽  
2012 ◽  
Vol 78 (11) ◽  
Author(s):  
JL Ríos ◽  
A Martí ◽  
I Andújar ◽  
RM Giner ◽  
MC Recio

2021 ◽  
Vol 9 (2) ◽  
pp. 370
Author(s):  
Hyunjoon Park ◽  
Soyoung Yeo ◽  
Seokwon Kang ◽  
Chul Sung Huh

The role of the gut microbiota in the pathogenesis of inflammatory bowel disease (IBD) has been in focus for decades. Although metagenomic observations in patients/animal colitis models have been attempted, the microbiome results were still indefinite and broad taxonomic presumptions were made due to the cross-sectional studies. Herein, we conducted a longitudinal microbiome analysis in a dextran sulfate sodium (DSS)-induced colitis mouse model with a two-factor design based on serial DSS dose (0, 1, 2, and 3%) and duration for 12 days, and four mice from each group were sacrificed at two-day intervals. During the colitis development, a transition of the cecal microbial diversity from the normal state to dysbiosis and dynamic changes of the populations were observed. We identified genera that significantly induced or depleted depending on DSS exposure, and confirmed the correlations of the individual taxa to the colitis severity indicated by inflammatory biomarkers (intestinal bleeding and neutrophil-derived indicators). Of note, each taxonomic population showed its own susceptibility to the changing colitis status. Our findings suggest that an understanding of the individual susceptibility to colitis conditions may contribute to identifying the role of the gut microbes in the pathogenesis of IBD.


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